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被甲磺酸甲酯或紫外线损伤的噬菌体T7的可诱导再激活。

Inducible reactivation of bacteriophage T7 damaged by methyl methanesulfonate or UV light.

作者信息

Dodson L A, Masker W E

出版信息

J Bacteriol. 1983 Oct;156(1):13-8. doi: 10.1128/jb.156.1.13-18.1983.

DOI:10.1128/jb.156.1.13-18.1983
PMID:6352671
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC215045/
Abstract

We examined the effects of host mutations affecting "SOS"-mediated UV light reactivation on the survival of bacteriophage T7 damaged by UV light or methyl methanesulfonate (MMS). Survival of T7 alkylated with MMS was not affected by the presence of plasmid pKM101 or by a umuC mutation in the host. The survival of UV light-irradiated T7 was similar in umuC+ and umuC strains but was slightly enhanced by the presence of pKM101. When phage survival was determined on host cells preirradiated with a single inducing dose of UV light, these same strains permitted higher survival than that seen with noninduced cells for both UV light- and MMS-damaged phage. The extent of T7 reactivation was approximately proportional to the UV light inducing dose inflicted upon each bacterial strain and was dependent upon phage DNA damage. Enhanced survival of T7 after exposure to UV light or MMS was also observed after thermal induction of a dnaB mutant. Thus, lethal lesions introduced by UV light or MMS are apparently repaired more efficiently when host cells are induced for the SOS cascade, and this inducible reactivation of T7 is umuC+ independent.

摘要

我们研究了宿主突变对“SOS”介导的紫外线光复活作用的影响,该作用涉及受紫外线或甲磺酸甲酯(MMS)损伤的噬菌体T7的存活情况。用MMS烷基化处理的T7的存活不受质粒pKM101的存在或宿主中umuC突变的影响。紫外线照射的T7在umuC +和umuC菌株中的存活情况相似,但pKM101的存在会使其存活略有增加。当在预先用单一诱导剂量紫外线照射的宿主细胞上测定噬菌体存活时,对于紫外线和MMS损伤的噬菌体,这些相同的菌株比未诱导细胞的存活情况更好。T7的复活程度大约与施加于每个细菌菌株的紫外线诱导剂量成正比,并且取决于噬菌体DNA损伤。在热诱导dnaB突变体后,也观察到T7在暴露于紫外线或MMS后的存活增加。因此,当宿主细胞被诱导进入SOS级联反应时,由紫外线或MMS引入的致死性损伤显然能更有效地被修复,并且这种T7的诱导性复活不依赖于umuC +。

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本文引用的文献

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Induction of Mutations in a Bacterial Virus.细菌病毒中突变的诱导
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The SOS regulatory system of Escherichia coli.大肠杆菌的SOS调控系统。
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